CG&D
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gallimore, P. H.
Right arrow Articles by Grand, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gallimore, P. H.
Right arrow Articles by Grand, R. J.

Cell Growth & Differentiation, Vol 8, Issue 7 763-771, Copyright © 1997 by American Association of Cancer Research


ARTICLES

Differentiation is inhibited and a senescence pathway is activated when simian virus 40 tsA 58-transformed human retinoblasts are grown at the restrictive temperature

PH Gallimore, PS Lecane, B Hann and RJ Grand
Cancer Research Campaign Institute for Cancer Studies, Medical School, University of Birmingham, Edgbaston, United Kingdom.

Neonatal human retina cells transformed by the SV40 tumor antigens were shown to leave the cell cycle and differentiate following treatment with agents that raise intracellular levels of cyclic AMP. This was true for both precrisis and immortal cell lines. However, with time, some of the differentiated retinoblasts withdrew neurites and returned to the cell cycle. Attempts to inhibit this process by developing cell lines transformed using SV tsA 58 with a temperature-sensitive phenotype for growth did not enhance but inhibited retinoblast-differentiating capacity. Growth restriction at the nonpermissive temperature was found to activate a senescence pathway. We propose that at the nonpermissive temperature, stable SV40 T-ag-p53 complexes fragment releasing p53, which transactivates p21waf1/cip1/sdi1 with the subsequent accumulation of p21 culminating in growth inhibition and senescence.


This article has been cited by other articles:


Home page
Cell Growth Differ.Home page
E. C. Goodwin and D. DiMaio
Induced Senescence in HeLa Cervical Carcinoma Cells Containing Elevated Telomerase Activity and Extended Telomeres
Cell Growth Differ., November 1, 2001; 12(11): 525 - 534.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1997 by the American Association of Cancer Research.